title: Caspase-14 overexpression in hairless mice is not involved in utricle formation.
abstract: Loss of functional hairless (HR) transcriptional repressor leads to utricle formation and congenital hair loss both in mice and men. Studies in mice have shown that this is preceded by overexpression of caspase-14 at the infundibulum in the hair follicle before conversion to utricle occurs. In this report, we show that HR regulates caspase-14 expression dependent on its interaction with histone deacetylases, implicating chromatin remodelling in the transcriptional regulation of caspase-14. However, crossing hairless mutant mice with caspase-14-deficient mice revealed that caspase-14 overexpression is not the cause of utricle formation.
authors.forename: Michael
authors.initials: M
authors.lastname: Devos
authors.forename: Philippe
authors.initials: P
authors.lastname: De Groote
authors.forename: Barbara
authors.initials: B
authors.lastname: Gilbert
authors.forename: Inge
authors.initials: I
authors.lastname: Bruggeman
authors.forename: Kirsten
authors.initials: K
authors.lastname: Leurs
authors.forename: Saskia
authors.initials: S
authors.lastname: Lippens
authors.forename: Peter
authors.initials: P
authors.lastname: Vandenabeele
authors.forename: Wim
authors.initials: W
authors.lastname: Declercq
mesh_terms: D000818:Animals; D020169:Caspases / Q000378:metabolism*; D002460:Cell Line; D003433:Crosses, Genetic; D015971:Gene Expression Regulation, Enzymologic; D018859:Hair Follicle / Q000502:physiology*; D006655:Histone Deacetylases / Q000378:metabolism*; D006801:Humans; D051379:Mice; D008812:Mice, Hairless; D008822:Mice, Transgenic; D008856:Microscopy, Fluorescence; D009154:Mutation; D010641:Phenotype; D012444:Saccule and Utricle / Q000502:physiology*
chemical_list: C506446:CASP14 protein, human; C506449:Casp14 protein, mouse; D020169:Caspases; D006655:Histone Deacetylases